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Leukoplakia

LeukoplakiaEtiology • Essentially unknown, although many cases related to use of
tobacco or areca nut in its various formulations • Other possible factors include nutritional deficiency (iron, vitamin
A) and infection (Candida albicans, human papillomavirus). Clinical Presentation
• An idiopathic white (sometimes white-and-red) patch • Most common on lip, gingiva, buccal mucosa • Increased risk of dysplasia or carcinoma when occurring on

tongue, floor of mouth, vermilion portion of lip • Clinical subsets include homogeneous, verrucous, speckled,
and proliferative verrucous leukoplakia (proliferative form may be multiple and persistent)
• Cases may advance or regress unpredictably—reflective of a dynamic process
• Most occur in the fifth decade and beyond • Progress to dysplasia or malignancy may occur with little or no
change in clinical appearance. Diagnosis
• Performance of a biopsy is mandatory after elimination of any suspected causative factors
• Multiple biopsies of large lesions are needed to be performed due to microscopic heterogeneity within a single lesion.
Differential Diagnosis • Other white lesions
• Frictional keratosis • Burn (thermal/chemical) • Hyperplastic candidiasis • Lichen planus
• Genetic alterations (genodermatoses) • White sponge nevus • Hereditary benign intra- • Dyskeratosis epithelial dyskeratosis
Treatment • Excision modalities (surgery, laser ablation, cryosurgery) • Option to observe lesions diagnosed as benign hyperkeratosis
or mild dysplasia • Possibly photodynamic therapy • Topical cytotoxic drugs (bleomycin) remain experimental. • Recurrences common following apparent complete excision
Prognosis • Guarded • Observation with repeat biopsies to be performed
Prevention • Elimination of tobacco use and heavy alcohol consumption • Recurrences may be reduced by systemic retinoid therapy. • Possible dietary measures